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本文以秀丽隐杆线虫(C.elegans)为模式生物,通过测定microRNA-260(miR-260)编码基因敲除后(Deletion)突变株与野生株(N2)线虫寿命、生殖能力、进食能力和热刺激条件下的生存能力,研究miR-260在衰老进程中发挥的作用.利用线虫体内衰老相关关键基因表达量的分析,探讨miR-260干预衰老的可能分子机制.实验结果显示:miR-260突变株系相对于野生型线虫寿命缩短,子代数目减少,进食能力的衰弱速度减慢,热刺激条件下的生存条件能力降低.结论:miR-260敲除后总体上加快秀丽隐杆线虫突变体衰老的进程.其可能的分子机理为,miR-260主要通过影响饮食限制通路和TOR信号通路中共同关键基因eat-2以及JNK信号通路中的jnk-1基因等的表达来调控线虫的衰老进程.
In this paper, C. elegans was taken as a model organism and the life span, reproductive capacity, food intake capacity and survival of the nematode (Deletion) and wild type (N2) strains of microRNA-260 (miR- Heat stimulated conditions to study the role of miR-260 in the aging process.Using the analysis of the expression of key genes related to senescence in nematodes to explore the possible molecular mechanism of miR-260 intervention aging.Experimental results show that: miR-260 Compared with the wild-type C. elegans, the mutant strain had shorter lifespan, fewer progeny, slower feeding ability, and lower survival ability under thermal stimulation.Conclusion: After the miR-260 knockout, the mutation of C. elegans was accelerated The possible molecular mechanism of miR-260 is that miR-260 mainly regulates the senescence of nematodes by affecting the expression of the key gene eat-2 in the dietary and TOR signaling pathways, and the jnk-1 gene in the JNK signaling pathway process.